Nesfatin-1 attenuates injury in a rat model of myocardial infarction by targeting autophagy, inflammation, and apoptosis.

Nesfatin-1 plays an important role in the modulation of heart performance. However, it remains unclear how nesfatin-1 contributes to cell survival in acute myocardial infarction (MI). A rat model of MI was established via ligation of left anterior descending coronary artery (LAD) for 30 min and 20 µg/kg concentration of nesfatin-1 was intraperitoneally infused prior to reperfusion. At 24 h after reperfusion, oxidative stress markers, the expression of caspase3, beclin-1, pro-inflammatory cytokines, and the mRNA levels of Bax and Bcl-2 were evaluated. Results showed that nesfatin-1 markedly restored GSH content and SOD activity as well as reduced MDA levels compared to only the MI group (p < .05). Likewise, nesfatin-1 contributed to cell survival by inhibiting autophagy and apoptosis markers such as caspase3 and Bax (p < .05). Collectively, these findings support the idea that nasfatin-1 can be used as a good candidate to treat MI by targeting oxidative stress, apoptosis, and autophagy.